ライフサイエンスコーパス: rest level

1 about 30 microM (perhaps 100-1,000 times the resting level).

2 e regulation is contingent upon differential REST levels.

3 st depletions analyzed were to 8+/-6% of the resting level.

4 e SR depletion was to 20+/-10% (s.d.) of the resting level.

5 t membrane potentials more negative than the resting level.

6 uced yet always higher than the preocclusion resting level.

7 n, which is followed by a slow return to the resting level.

8 st and during exercise was below the control resting level.

9 [Ca2+]i has been completely restored to its resting level.

10 d to increase their precision estimates from resting levels.

11 lular Ca2+ that slowly recovered to baseline resting levels.

12 ollowed by a steady-state augmentation above resting levels.

13 cellular free calcium concentrations towards resting levels.

14 g [Ca2+]i elevations and clamping [Ca2+]i to resting levels.

15 e phagosome although [Ca(2+)](i) remained at resting levels.

16 in(-1), P<0.01) increased from the depressed resting levels.

17 l was able to effectively restore [Ca2+]i to resting levels.

18 lowed the recovery of [Ca(2+)](cyto) towards resting levels.

19 rophic muscles compared with those at normal resting levels.

20 ncrease in fluorescence (L(0)) compared with resting levels.

21 h internal calcium strongly buffered to near resting levels.

22 ackground discharge rates were comparable to resting levels.

23 ading to a slow return of Ca(i) and Na(i) to resting levels.

24 ased 8.4-fold (P = .002) and returned to the resting level 5 minutes after exercise, whereas the lact

25 rkinje cells fire a single type of spikes at resting level, a subset of small Purkinje cells fire sma

26 Sustained increase of REST levels after injury inhibits axon regeneration and

27 e, whereas reversal of glucose uptake toward resting levels after exercise/contraction was markedly f

28 ount for the depression of [Ca(2+)](i) below rest levels and the increased fall rate of [Ca(2+)](i) w

29 BA defects, leading to reduced intracellular resting levels and induced surface levels of CTLA-4.

30 y silencing the third copy of DYRK1A rescues Rest levels, and we demonstrate altered Rest expression

31 ion, the rate of actively returning force to resting levels, and passive release of force "relaxation

32 d (>30 s) even when [Ca(2+)](c) had regained resting levels, and was not prevented by kinase or phosp

33 regions of the adult nervous system, but how REST levels are regulated, and whether REST can still re

34 Thus, REST levels are titrated in mature peripheral neurons, i

35 he stereocilium and quickly falls toward the resting level as adaptation proceeds.

36 ithin 48 h of activation before returning to resting levels at 72 h.

37 responses to arterial pressure changes below resting levels but normal initial responses to upright t

38 olic Ca(2+) ([Ca(2+)](C)) was clamped to the resting level by a BAPTA-Ca(2+) mixture.

39 osolic Ca2+ concentration was clamped at the resting level by a high concentration of a selective Ca2

40 [Na+]i began to decline toward resting levels by 20 +/- 15 min (mean +/- S.D.) post-tra

41 tamine and LTC4 release and decreased toward resting levels by 30 min.

42 erable SN dopaminergic neurons displayed low REST levels compared with neighboring protected SN GABAe

43 ensuing 2 h, whereas ATP levels decayed to a resting level; consequently, resting extracellular UDP-g

44 suggest that by buffering [Ca(2+)](ER) near resting levels, CRT may prevent InsP(3) from depleting t

45 s monophasic but often undershot or overshot resting levels, depending on resting [Ca2+]c.

46 g intraterminal Ca2+ to approximately normal resting levels does not eliminate the modulation, sugges

47 Chelating of intracellular calcium below resting level drastically decreased cycling of nAChRs.

48 Finally, REST levels during ageing are closely correlated with co

49 their repression, associated with increased REST levels during aging, were found to be neuroprotecti

50 rease was due to a rise of intra-WPB pH from resting levels, estimated as pH 5.45+/-0.26 (s.d., n=144

51 s exhibited lower changes in MAP and HR from resting levels following termination of restraint.

52 ue, at least in part, to abnormally elevated REST levels in the ganglia because the axonal phenotype

53 , the entire axonal arborization returned to resting level in a spatially uniform manner during the D

54 n the illuminated zone, and then returned to resting level in approximately 10-15 s.

55 hibit the cyclase when free Ca2+ reaches its resting level in the dark.

56 sed animals exhibited similar increases from resting levels in HR during restraint.

57 h typically only ~1% being freely ionized at resting levels in most cells.

58 Surprisingly, NO reduced Ca(2)(+) resting levels in mouse cones, without evidence for dire

59 Rather, a [Ca2+] rise from resting levels is needed to achieve more than minimal cA

60 pharmacologically suppressed (p<0.05) supine rest levels of angiotensin II (-65%) and aldosterone (-7

61 sustained decrease in [Ca2+]i from the mean resting level of 114 nM to 58 nM.

62 ation in low [Cl] media as is NKCC1, but the resting level of activity is higher in h1r2A0.7 and acti

63 his discrepancy may be the difference in the resting level of Ang II, which may be lower in well-trai

64 -term, 15-30 nM rise of free Ca2+ (above the resting level of approximately 100 nM).

65 Furthermore in wild-type mice, the resting level of ATP correlates with organ-specific Sirt

66 This resting level of C2 inexcitability is attributable to it

67 The persistent elevation in the resting level of Ca(2+) induced by an accumulation of am

68 We conclude, therefore, that the lower resting level of Ca(2+) observed in EPA is due to a lowe

69 ling caused by a progressive increase in the resting level of Ca(2+), which may influence cognition b

70 They may therefore contribute to the resting level of channel inhibition in the intact cell.

71 hloride with prestin, we determined that the resting level of chloride in OHCs is near or below 10 mm

72 GABAergic system, it is conceivable that the resting level of cortical GABAergic tone directly relate

73 The resting level of cytosolic Ca2+ in DC-3F/TG2 cells was 2

74 The resting level of free calcium ion concentration in the m

75 take capacity are impaired, and an increased resting level of free intracellular Ca(2+) is accompanie

76 The resting level of intracellular Ca2+ concentrations also

77 At the same time the resting level of intracellular calcium falls, the restin

78 larizing phase removes a small degree of the resting level of Na(+) channel inactivation.

79 Resting levels of angiotensin II, aldosterone, vasopress

80 Rather, PDE5 inhibition decreased resting levels of ATP, phosphocreatine and myoglobin, su

81 The rise in resting levels of Ca(2+) may not alter the processes of

82 y and possibly other EF-hand proteins at the resting levels of Ca(2+).

83 release without increasing [Ca2+]i, although resting levels of calcium are required, suggesting alter

84 In unanesthetized normal sheep, resting levels of cortical and medullary tissue PO2 were

85 ition and thus do not contribute markedly to resting levels of CSNA and HR, but when disinhibited, th

86 n could disassemble myosin filaments even at resting levels of cytoplasmic [Ca(2+)].

87 thin 10% and were associated with equivalent resting levels of electromyographic (EMG) activity.

88 d repetitive Ca(2+) waves in the presence of resting levels of free [Mg(2+)]cyto (1 mM).

89 TGgamma2N488I hearts had normal resting levels of high-energy phosphates and could impro

90 ing restraint were due to the differences in resting levels of HR, since both control and chronically

91 ows 2-Cys Prxs to act as floodgates, keeping resting levels of hydrogen peroxide low, while permittin

92 n to its homeostatic role of maintaining low resting levels of intracellular calcium ([Ca2+](i)), the

93 to morphology, neurofilament expression, and resting levels of intracellular calcium.

94 he bovine isoform), rendering eNOS active at resting levels of intracellular calcium.

95 Finally, we report that resting levels of long-chain triacylglycerols in mitocho

96 Resting levels of LTs were greater in esophagitis than i

97 d Phase 2 were a result of the elevations in resting levels of MAP, but even when differences in rest

98 The resting levels of MGF were significantly (approximately

99 Resting levels of neutrophil phospholipase A2 activity i

100 normal left ventricular function, and normal resting levels of NT-pro-BNP and BNP who were referred f

101 Resting levels of O2 in the rodent brain varied between

102 ents with focal limb dyskinesias showed that resting levels of regional cerebral blood flow after ora

103 responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have

104 No difference was observed between the resting levels of the two isoforms between the two subje

105 sed by agonist-stimulation, recovered to the resting level on addition of 8-Br-cGMP.

106 uff occlusion sustained blood pressure above resting levels only when the leg had intact sensation.

107 tely 20-30 s with thrombin present either to resting levels or to a maintained elevated level of 2.0

108 The higher REST levels result in lower levels of target genes, indi

109 g, low plateau, then [Ca2+]i returned to the resting level slowly.

110 by 2 degrees C with CO(2) /pH normalized to resting levels, there was a marked cerebral uptake of mi

111 plication is that an increase in ICAM-1 from resting levels to those on inflamed endothelium effectiv

112 Consistent with a protective role, REST levels were reduced in patient induced pluripotent

113 t neuronal differentiation genes even though REST levels were unaffected.

114 ls were unchanged in the training group, but resting levels were significantly (p < 0.001) reduced (a

115 levels of MAP, but even when differences in resting levels were taken into account, HR remained elev

116 es in endoplasmic reticulum calcium near the resting level, whereas a threshold of calcium depletion

117 ic Ca2+ concentration to the pre-stimulation resting level, which was attained long before the endopl

118 ccur with slight elevations of calcium above resting levels, which implies that inhibition should be

119 is prevented by buffering [Ca(2+)] at normal resting levels while in wildtype PNs mGluR1 EPSCs are en

120 etics of other early signals and returned to resting levels while nonspecific desensitization remaine

121 [Ca2+]i returned to resting level with a time course that, like endocytosis,

122 CETNO decreased and V NO increased above resting levels with increasing exercise intensity during